Cyclic AMP as the intracellular message in Beta-adrenergic mediated processes including lipolysis is widely accepted. More recently, the complexity of signals or inputs that govern the physiological response e.g. lipolysis to a hormone including the catecholamines has become obvious. Unless a certain threshold perfusate (Ca 2 ion) is present, isoproterenol will not activate lipolysis in heart even though cellular cyclic AMP is elevated. In further investigating the role of Ca 2 ion in myocardial metabolism including triglyceride breakdown, alpha-adrenergic stimulation (phenylephrine in the presence of propranolol) of the isolated perfused rat heart will be examined. A positive inotropic effect without an elevation of cellular cyclic AMP has been shown to occur with alpha-adrenergic stimulation which is augmented in hypothyroidism. A possible interaction of permissive hormones (glucocorticoids, thyroid hormones) with catecholamine-activated lipolysis in the perfused heart will also be investigated. For example, thyroid function will be altered in the rat e.g. propylthiouracil-hypothyroidism and then the responsiveness of myocardial metabolism including lipolysis to catecholamines will be monitored in the isolated perfused heart. Since raising perfusate (Ca 2 ion) has been shown to overcome the block in epinephrine-stimulated glycogenolysis that exists in perfused hearts from adrenalectomized rats, it would be expected that a similar finding would be observed in catecholamine activated myocardial lipolysis. Deficiencies in catecholamine-mediated processes in both heart and adipose tissue in animal models of diabetes have been shown yet the factors responsible remain unclear. Appreciation of alterations in pancreatic hormone secretion and action in diabetes is apparent, yet the exact function of the counter-regulatory hormones e.g. glucocorticoids in the syndrome including defects in the Beta-adrenergic mediated processes has yet to be delineated.